J Neuroimmunol. 2004 Mar;148(1-2):1-10
Zhang GX, Yu S, Gran B, Li J, Calida D, Ventura E, Chen X, Rostami A.
Department of Neurology, Thomas Jefferson University, 1025 and Walnut Street, Suite 310, Philadelphia, PA 19107-5083, USA.
To characterize T cell and antibody responses in remitting-relapsing experimental autoimmune encephalomyelitis (RR-EAE), we compared myelin oligodendrocyte glycoprotein (MOG)-induced RR-EAE in C57BL/6 (B6)xSJL (F1) mice and chronic-progressive EAE (CP-EAE) in B6 mice at week 8 p.i. when clinical scores were comparable.
Although these two strains exhibited similar inflammation/demyelination pattern and MOG-induced T cell responses, RR-EAE mice produced significantly higher levels of anti-MOG IgG1/IgG2a antibodies.
Further, lymphocytes of RR-EAE mice proliferated vigorously to the secondary epitope myelin basic protein (MBP) 1-11.
These results support a potential involvement of anti-MOG antibodies and epitope spreading in T cell responses in the development of MOG-induced RR-EAE model.